Hi,
this article also gives a nice explanation of the mechanisms behind diabetic
neuropathy. I  _think_  the same explanation can be given for the diabetic
neuropathy effecting (my) feet. It also explains why anti-oxidants like
Alpha Lipoic Acid work well for diabetic neuropathy.

Here is the Pubmed Link :

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16400026&query_hl=1&itool=pubmed_docsum

Here is the Link for the press release :

http://www.mcg.edu/news/2006NewsRel/Liou022706.html

Here is an abstract from the press release :

We are studying the role of cannabinoid receptors in our body and trying to
modulate them so we can defend against diabetic retinopathy. Diabetic
retinopathy is the leading cause of blindness in working-age adults and
affects nearly 16 million Americans.

High glucose levels resulting from unmanaged diabetes set in motion a
cascade ultimately causing the oxygen-deprived retina to grow more blood
vessels. Ironically, the leaky surplus of vessels can ultimately destroy
vision.

Cannabinoid receptors are found throughout the body and endogenous
cannabinoids are produced to act on them. Their function is very different
from organ to organ but in the central nervous system, cannabinoid receptors
are responsible for the neutralization process that should occur after a
nerve impulse is finished.

Nerves come together at a point of communication called a synapse. Glutamate
is a neurotransmitter that excites these nerves to action at their point of
communication.There are also inhibitory neurotransmitters such as GABA.
Endogenous cannabinoids help balance the excitation and inhibition, at least
until oxygen gets scarce.

In the face of inadequate oxygen, or ischemia - another hallmark of
diabetes - nerve endings start producing even more glutamate, setting in
motion an unhealthy chain of events. Pumps that keep the right substances
inside or outside of cells start to malfunction. Excess nitric oxide and
superoxides are produced, which are toxic to the cells. Another irony is the
heightened activity increases the retina's need for oxygen. We are talking
about nerve cell death.In the retina, if a lot of our nerve cells die, our
vision is directly affected."

And that's not all that goes wrong in the nerve-packed retina. Glial cells,
which support nerve cells by supplying nutrients and oxygen, are closely
attuned to their charges. When they sense something is amiss, microglia, one
type of glial cells, start eating the dying nerve cells.

Microglial cells become voracious. They eat dying nerve cells, making the
whole thing irreversibly bad. Interestingly, the body start producing more
endogenous cannabinoids to stop the role reversal, then produces an enzyme
to destroy the cannabinoids because of concern there are too many of them.
The same thing happens in the brain after a stroke.Long before all these
blood vessels start growing, the partnership between glial cells and nerve
cells starts breaking down.

That's why cannabidiol, an antioxidant, may help save the retina. Test-tube
studies by others, as well as Dr. Liou's pilot studies in diabetic animal
models show cannabidiol works to interrupt essentially all these destructive
points of action.

What we believe cannabidiol does is go in here as an antioxidant to
neutralize the toxic superoxides. Number two, it inhibits the
self-destructive system and allows the self-produced endogenous cannabinoids
to stay there longer by inhibiting the enzyme that destroys them.
Cannabidiol also helps keep microglial cells from turning on nerve cells by
inhibiting cannabinoid receptors on microglial cells that are at least
partially responsible for their ability to destroy rather than support the
cells.

Cannabinoids are trying to ease the situation on both sides. They help save
the neuron and, at the same time, make sure the microglial cells stay in
microglial form. How good do you want a drug to be?" Dr. Liou says.

Dr. Gregory I. Liou, molecular biologist at the Medical College of Georgia ,
hopes the compound in marijuana may one day be given along with insulin to
stop the early changes that set the stage for damaged or destroyed vision.

hth
Gys , T2